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Summary Sleepwalking and related parasomnias are thought to result from incomplete awakenings out of non‐rapid eye movement (non‐REM) sleep. Non‐REM parasomnia behaviours have been described as unconscious and automatic, or related to vivid, dream‐like conscious experiences. Similarly, some observations have suggested that patients are unresponsive during episodes, while others that they can interact with their surroundings. To better grasp and characterise the full spectrum of consciousness and environmental (dis)connection associated with behavioural episodes, 35 adult patients with non‐REM sleep parasomnias were interviewed in‐depth about their experiences. The level of consciousness during parasomnia episodes was reported to be variable both within and between individuals, ranging from minimal or absent consciousness and largely automatic behaviours (frequently/always present in 36% of patients) to preserved conscious experiences characterised by delusional thinking to varying degrees of specificity (65%), often about impending danger, variably formed, uni‐ or multisensory hallucinations (53%), impaired insight (77%), negative emotions (75%), and variable, but often pronounced, amnesia (30%). Patients described their experiences as a dream scene during which they felt awake (“awake dreaming”). The surroundings were either realistically perceived, misinterpreted (in the form of perceptual illusions or misidentifications of people), or entirely hallucinated as a function of the prevailing delusion. These observations suggest that the level of consciousness, amnesia and sensory disconnection during non‐REM parasomnia episodes is variable and graded. In their full‐fledged expression, non‐REM parasomnia experiences feature several core features of dreams. They therefore represent a valuable model for the study of consciousness, sleep‐related sensory disconnection and dreaming. [ABSTRACT FROM AUTHOR]

Summary: Non‐rapid eye movement parasomnia disorders, also called disorders of arousal, are characterized by abnormal nocturnal behaviours, such as confusional arousals or sleep walking. Their pathophysiology is not yet fully understood, and objective diagnostic criteria are lacking. It is known, however, that behavioural episodes occur mostly in the beginning of the night, after an increase in slow‐wave activity during slow‐wave sleep. A better understanding of the prospect of such episodes may lead to new insights in the underlying mechanisms and eventually facilitate objective diagnosis. We investigated temporal dynamics of transitions from slow‐wave sleep of 52 patients and 79 controls. Within the patient group, behavioural and non‐behavioural N3 awakenings were distinguished. Patients showed a higher probability to wake up after an N3 bout ended than controls, and this probability increased with N3 bout duration. Bouts longer than 15 min resulted in an awakening in 73% and 34% of the time in patients and controls, respectively. Behavioural episodes reduced over sleep cycles due to a reduction in N3 sleep and a reducing ratio between behavioural and non‐behavioural awakenings. In the first two cycles, N3 bouts prior to non‐behavioural awakenings were significantly shorter than N3 bouts advancing behavioural awakenings in patients, and N3 awakenings in controls. Our findings provide insights in the timing and prospect of both behavioural and non‐behavioural awakenings from N3, which may result in prediction and potentially prevention of behavioural episodes. This work, moreover, leads to a more complete characterization of a prototypical hypnogram of parasomnias, which could facilitate diagnosis. [ABSTRACT FROM AUTHOR]

Summary: Dreams were a subject of interest to philosophers thinking about the connection between the mind and the body in the nineteenth century. Many scholars have pointed out that the mind and the body were intimately linked and affected each other. Although science was on its way to becoming more technical and numbers focused in its investigatory practices, medical students and other physician‐philosophers investigated the nature of sleep and dreams. Medical students and advanced researchers speculated on the nature of consciousness and mused on where the mind travels to during the sleep processes. Other romantic figures like Dr Polydori speculated on the nature of sleep walking in their medical dissertations. Dreams also had a powerful moral and motivational component, as dreams and activities in dreams, drove people like Benjamin Rush to embrace abolition. Other promoters of abolition used the nature of dreams to discusses the dreadfulness and suffering of slavery. [ABSTRACT FROM AUTHOR]

Summary: Disorders of arousal (DOA) is an umbrella term initially covering classical sleepwalking, sleep terrors, and confusional arousals, and now including a wider spectrum of specialised forms of non rapid eye movement (non REM) parasomnias such as sexsomnia, sleep‐related eating disorder, and sleep‐related choking syndrome. Growing evidence has shown that DOA are not restricted to children but are also prevalent in adults (2%–4% of the adult population). While DOA run in family, genetics studies remain scarce and inconclusive. In addition to the risk of injury on themselves and others (including sexual assaults in sexsomnia), adults with DOA frequently suffer from excessive daytime sleepiness, pain, and altered quality of life. The widespread view of DOA as automatic and amnesiac behaviours has now been challenged by subjective (dream reports) and objective (dream‐enacting behaviours documented on video‐polysomnography) observations, suggesting that sleepwalkers are 'dream walking' during their episodes. Behavioural, experiential, cognitive, and brain (scalp electroencephalography [EEG], stereo‐EEG, high density‐EEG, functional brain imaging) data converge in showing a dissociated pattern during the episodes. This dissociated pattern resembles the new concept of local arousal with a wake‐like activation in motor and limbic regions and a preserved (or even increased) sleep intensity over a frontoparietal network. EEG and behavioural criteria supporting the DOA diagnosis with high sensitivity and specificity are now available. However, treatment is still based on controlling priming and precipitating factors, as well as on clinicians' personal experience with sedative drugs. Placebo‐controlled trials are needed to improve patients' treatment. DOA deserve more attention from sleep researchers and clinicians. [ABSTRACT FROM AUTHOR]

Summary: Sleepwalking is a common non‐rapid eye movement (NREM) parasomnia and a significant cause of sleep‐related injuries. While evidence suggest that the occurrence of this condition is partly determined by genetic factors, its pattern of inheritance remains unclear, and few molecular studies have been conducted. One promising candidate is the adenosine deaminase (ADA) gene. Adenosine and the ADA enzyme play an important role in the homeostatic regulation of NREM sleep. In a single sleepwalking family, genome‐wide analysis identified a locus on chromosome 20, where ADA lies. In this study, we examined if variants in the ADA gene were associated with sleepwalking. In total, 251 sleepwalking patients were clinically assessed, and DNA samples were compared to those from 94 unaffected controls. Next‐generation sequencing of the whole ADA gene was performed. Bio‐informatic analysis enabled the identification of variants and assessed variants enrichment in our cohort compared to controls. We detected 25 different coding and non‐coding variants, of which 22 were found among sleepwalkers. None were enriched in the sleepwalking population. However, many missense variants were predicted as likely pathogenic by at least two in silico prediction algorithms. This study involves the largest sleepwalking cohort in which the role of a susceptibility gene was investigated. Our results did not reveal an association between ADA gene and sleepwalking, thus ruling out the possibility of ADA as a major genetic factor for this condition. Future work is needed to identify susceptibility genes. [ABSTRACT FROM AUTHOR]

Summary: Disorders of arousals are common sleep disorders characterized by complex motor behaviours that arise episodically out of slow‐wave sleep. Psychological distress has long been associated with disorders of arousal, but this link remains controversial, especially in children and adolescents. The aim of this multi‐centre study was to characterize behavioural and emotional problems in a sample of children/adolescents with disorders of arousal, and to explore their relationship with the severity of nocturnal episodes. The parents of 41 children/adolescents with a diagnosis of disorders of arousal (11.5 ± 3.3 years old, 61% males) and of a group of 41 age‐ and gender‐matched control participants filled in the Child Behavior Checklist, along with the Sleep Disturbance Scale for Children and the Paris Arousal Disorders Severity Scale. Multilevel t‐tests revealed significantly higher total scores and sub‐scores of the Child Behavior Checklist for the patient group compared with the control group. Thirty‐four percent of the patients obtained pathological total scores, and 12% of them borderline scores. The severity of emotional/behavioural problems in the patient group was positively correlated with the severity of the nocturnal episodes. Interestingly, children/adolescents with disorders of arousal also obtained higher excessive daytime sleepiness and insomnia symptoms sub‐scores at the Sleep Disturbance Scale for Children. These results confirmed the hypothesis that behavioural/emotional problems are surprisingly common in children/adolescents with disorders of arousal. Further studies are warranted to investigate the causal relationship between pathological manifestations, subtler sleep abnormalities, and diurnal emotional/behavioural problems in children/adolescents with disorders of arousal. [ABSTRACT FROM AUTHOR]

To understand the mechanisms of N3 sleep interruptions in patients with sleepwalking episodes and/or sleep terrors (SW/ST), we evaluated whether autonomic reactions preceded or accompanied behavioural arousals from NREM sleep stage N3. In 20 adult patients with SW/ST and 20 matched controls without parasomnia, heart rate and pulse wave amplitude were measured beat‐to‐beat during the 10 beats preceding and during the 15 beats succeeding a motor arousal from N3 sleep. Respiratory rate and amplitude were measured during the same 25 successive beats. In patients with SW/ST, the N3 arousals were associated with a 33% increase in heart rate, a 57% decrease in pulse wave amplitude (indicating a major vasoconstriction), a 24% increase in respiratory rate and a doubling of respiratory amplitude. Notably, tachycardia and vasoconstriction started 4 s before motor arousals. A similar profile (tachycardia and vasoconstriction gradually increasing from the 4 s preceding arousal and post‐arousal increase of respiratory amplitude, but no polypnea) was also observed, with a lower amplitude, during the less frequent 38 quiet N3 arousals in control subjects. Parasomniac arousals were associated with greater tachycardia, vasoconstriction and polypnea than quiet arousals, with the same pre‐arousal gradual increases in heart rate and vasoconstriction. Autonomic arousal occurs 4 s before motor arousal from N3 sleep in patients with SW/ST (with a higher adrenergic reaction than in controls), suggesting that an alarming event during sleep (possibly a worrying sleep mentation or a local subcortical arousal) causes the motor arousal. [ABSTRACT FROM AUTHOR]

This study sought to determine if there is any overlap between the two major non-rapid eye movement and rapid eye movement parasomnias, i.e. sleepwalking/sleep terrors and rapid eye movement sleep behaviour disorder. We assessed adult patients with sleepwalking/sleep terrors using rapid eye movement sleep behaviour disorder screening questionnaires and determined if they had enhanced muscle tone during rapid eye movement sleep. Conversely, we assessed rapid eye movement sleep behaviour disorder patients using the Paris Arousal Disorders Severity Scale and determined if they had more N3 awakenings. The 251 participants included 64 patients with rapid eye movement sleep behaviour disorder (29 with idiopathic rapid eye movement sleep behaviour disorder and 35 with rapid eye movement sleep behaviour disorder associated with Parkinson's disease), 62 patients with sleepwalking/sleep terrors, 66 old healthy controls (age-matched with the rapid eye movement sleep behaviour disorder group) and 59 young healthy controls (age-matched with the sleepwalking/sleep terrors group). They completed the rapid eye movement sleep behaviour disorder screening questionnaire, rapid eye movement sleep behaviour disorder single question and Paris Arousal Disorders Severity Scale. In addition, all the participants underwent a video-polysomnography. The sleepwalking/sleep terrors patients scored positive on rapid eye movement sleep behaviour disorder scales and had a higher percentage of 'any' phasic rapid eye movement sleep without atonia when compared with controls; however, these patients did not have higher tonic rapid eye movement sleep without atonia or complex behaviours during rapid eye movement sleep. Patients with rapid eye movement sleep behaviour disorder had moderately elevated scores on the Paris Arousal Disorders Severity Scale but did not exhibit more N3 arousals (suggestive of non-rapid eye movement parasomnia) than the control group. These results indicate that dream-enacting behaviours (assessed by rapid eye movement sleep behaviour disorder screening questionnaires) are commonly reported by sleepwalking/sleep terrors patients, thus decreasing the questionnaire's specificity. Furthermore, sleepwalking/sleep terrors patients have excessive twitching during rapid eye movement sleep, which may result either from a higher dreaming activity in rapid eye movement sleep or from a more generalised non-rapid eye movement/rapid eye movement motor dyscontrol during sleep. [ABSTRACT FROM AUTHOR]

Sleepwalkers often complain of excessive daytime somnolence. Although excessive daytime somnolence has been associated with cognitive impairment in several sleep disorders, very few data exist concerning sleepwalking. This study aimed to investigate daytime cognitive functioning in adults diagnosed with idiopathic sleepwalking. Fifteen sleepwalkers and 15 matched controls were administered the Continuous Performance Test and Stroop Colour-Word Test in the morning after an overnight polysomnographic assessment. Participants were tested a week later on the same neuropsychological battery, but after 25 h of sleep deprivation, a procedure known to precipitate sleepwalking episodes during subsequent recovery sleep. There were no significant differences between sleepwalkers and controls on any of the cognitive tests administered under normal waking conditions. Testing following sleep deprivation revealed significant impairment in sleepwalkers' executive functions related to inhibitory control, as they made more errors than controls on the Stroop Colour-Word Test and more commission errors on the Continuous Performance Test. Sleepwalkers' scores on measures of executive functions were not associated with self-reported sleepiness or indices of sleep fragmentation from baseline polysomnographic recordings. The results support the idea that sleepwalking involves daytime consequences and suggest that these may also include cognitive impairments in the form of disrupted inhibitory control following sleep deprivation. These disruptions may represent a daytime expression of sleepwalking's pathophysiological mechanisms. [ABSTRACT FROM AUTHOR]

In order to evaluate verbal memory consolidation during sleep in subjects experiencing sleepwalking or sleep terror, 19 patients experiencing sleepwalking/sleep terror and 19 controls performed two verbal memory tasks (16-word list from the Free and Cued Selective Reminding Test, and a 220- and 263-word modified story recall test) in the evening, followed by nocturnal video polysomnography ( n = 29) and morning recall (night-time consolidation after 14 h, n = 38). The following morning, they were given a daytime learning task using the modified story recall test in reverse order, followed by an evening recall test after 9 h of wakefulness (daytime consolidation, n = 38). The patients experiencing sleepwalking/sleep terror exhibited more frequent awakenings during slow-wave sleep and longer wakefulness after sleep onset than the controls. Despite this reduction in sleep quality among sleepwalking/sleep terror patients, they improved their scores on the verbal tests the morning after sleep compared with the previous evening (+16 ± 33%) equally well as the controls (+2 ± 13%). The performance of both groups worsened during the daytime in the absence of sleep (−16 ± 15% for the sleepwalking/sleep terror group and −14 ± 11% for the control group). There was no significant correlation between the rate of memory consolidation and any of the sleep measures. Seven patients experiencing sleepwalking also sleep-talked during slow-wave sleep, but their sentences were unrelated to the tests or the list of words learned during the evening. In conclusion, the alteration of slow-wave sleep during sleepwalking/sleep terror does not noticeably impact on sleep-related verbal memory consolidation. [ABSTRACT FROM AUTHOR]

Sleepwalkers have been shown to have an unusually high number of arousals from slow wave sleep and lower slow wave activity ( SWA) power during the night than controls. Because sleep deprivation increases the frequency of slow wave sleep ( SWS) arousals in sleepwalkers, it may also affect the expression of the homeostatic process to a greater extent than shown previously. We thus investigated SWA power as well as slow wave oscillation ( SWO) density in 10 sleepwalkers and nine controls at baseline and following 38 h of sleep deprivation. There was a significant increase in SWA during participants' recovery sleep, especially during their second non-rapid eye movement ( NREM) period. SWO density was similarly increased during recovery sleep's first two NREM periods. A fronto-central gradient in SWA and SWO was also present on both nights. However, no group differences were noted on any of the 2 nights on SWA or SWO. This unexpected result may be related to the heterogeneity of sleepwalkers as a population, as well as our small sample size. SWA pressure after extended sleep deprivation may also result in a ceiling effect in both sleepwalkers and controls. [ABSTRACT FROM AUTHOR]

Small urinary protein loss (low-grade albuminuria or microalbuminuria) may reflect altered permeability of the glomerular filtration barrier. In the present study, it was hypothesized that children with obstructive sleep apnea have an increased risk of microalbuminuria compared with control subjects without sleep-disordered breathing. Albumin-to-creatinine ratio was measured in morning spot urine specimens collected from consecutive children with or without snoring who were referred for polysomnography. Three groups were studied: (i) control subjects (no snoring, apnea-hypopnea index < 1 episode h−1; n = 31); (ii) mild obstructive sleep apnea (snoring, apnea-hypopnea index = 1-5 episodes h−1; n = 71); and (iii) moderate-to-severe obstructive sleep apnea (snoring, apnea-hypopnea index > 5 episodes∙h−1; n = 27). Indications for polysomnography in control subjects included nightmares, somnambulism and morning headaches. An albumin-to-creatinine ratio > median value in the control group (1.85 mg of albumin per g of creatinine) was defined as elevated. Logistic regression analysis revealed that children with moderate-to-severe obstructive sleep apnea, but not those with mild obstructive sleep apnea, had increased risk of elevated albumin-to-creatinine ratio relative to controls (reference) after adjustment for age, gender and presence of obesity: odds ratio 3.8 (95% confidence interval 1.1-12.6); P = 0.04 and 1.5 (0.6-3.7); P > 0.05, respectively. Oxygen desaturation of hemoglobin and respiratory arousal indices were significant predictors of albumin-to-creatinine ratio ( r = 0.31, P = 0.01; and r = 0.43, P < 0.01, respectively). In conclusion, children with moderate-to-severe obstructive sleep apnea are at significantly higher risk of increased low-grade excretion of albumin in the morning urine as compared with control subjects without obstructive sleep apnea. These findings may reflect altered permeability of the glomerular filtration barrier related to nocturnal hypoxemia and sympathetic activation which are induced by obstructive sleep apnea. [ABSTRACT FROM AUTHOR]

An increasing number of criminal cases have claimed the defendant to be in a state of sleepwalking or related disorders induced by high quantities of alcohol. Sleepwalkers who commit violent acts, sexual assaults and other criminal acts are thought to be in a state of automatism, lacking conscious awareness and criminal intent. They may be acquitted in criminal trials. On the other hand, criminal acts performed as the result of voluntary alcohol intoxication alone cannot be used as a complete defense. The alcohol-induced sleepwalking criminal defense is most often based on past clinical or legal reports that ingestion of alcohol directly ‘triggers’ sleepwalking or increased the risk of sleepwalking by increasing the quantity of slow wave sleep (SWS). A review of the sleep medicine literature found no sleep laboratory studies of the effects of alcohol on the sleep of clinically diagnosed sleepwalkers. However, 19 sleep laboratory studies of the effects of alcohol on the sleep of healthy non-drinkers or social drinkers were identified with none reporting a change in SWS as a percentage of total sleep time. However, in six of 19 studies, a modest but statistically significant increase in SWS was found in the first 2–4 h. Among studies of sleep in alcohol abusers and abstinent abusers, the quantity and percentage of SWS was most often reduced and sometimes absent. Claims that direct alcohol provocation tests can assist in the forensic assessment of these cases found no support of any kind in the medical literature with not a single report of testing in normative or patient groups and no reports of validation testing of any sort. There is no direct experimental evidence that alcohol predisposes or triggers sleepwalking or related disorders. A legal defense of sleepwalking resulting from voluntarily ingested alcohol should be consistent with the current state of art sleep science and meet generally accepted requirements for the diagnosis of sleepwalking and other parasomnias. [ABSTRACT FROM AUTHOR]

Early studies found that electroencephalographic (EEG) recordings during somnambulistic episodes were characterized by a combination of alpha, theta, and delta frequencies, without evidence of clear wakefulness. Three postarousal EEG patterns associated with slow-wave sleep (SWS) arousals were recently identified in adults with sleepwalking and sleep tenors. The goal of the present study was to evaluate the distribution of these postarousal EEG patterns in 10 somnambulistic patients (three males, seven females, mean age: 25.1, SD: 4.1) evaluated at baseline and following 38 h of sleep deprivation. A total of 44 behavioral arousals were recorded in the laboratory; seven episodes at baseline (five from SWS, two from stage 2 sleep) and 37 episodes during recovery sleep (30 from SWS, seven from stage 2 sleep). There was no significant difference in the distribution of postarousal EEG patterns identified during baseline and recovery sleep. One pattern, comprised of diffuse rhythmic and synchronous delta activity, was preferentially associated with relatively simple behavioral episodes but did not occur during episodes from stage 2 sleep. Overall, delta activity was detected in 48% of the behavioral episodes from SWS and in 22% of those from stage 2. There was no evidence of complete awakening during any of the episodes. The results support the view of somnambulism as a disorder of arousal and suggest that sleepwalkers' atypical arousal reactions can manifest themselves in stage 2 sleep in addition to SWS. [ABSTRACT FROM AUTHOR]

Human foetuses and newborns smile first during sleep, before they smile while awake and interacting with caregivers. Whether smiling persists during adult sleep, and expresses inner joy, is yet unknown. Smiles were looked for during night‐time video‐polysomnography combined with electromyography of the zygomatic and orbicularis oculi muscles in 100 controls, 22 patients with sleepwalking and 52 patients with rapid eye movement (REM) sleep behaviour disorder. Autonomous reactions (heart rate and level of vasoconstriction) and the presence of rapid eye movements were examined during smiles and laughs. On visual examination of the face video clips synchronous with zygomatic contraction, 8% of controls smiled while asleep (7% in REM sleep and 1% in non‐REM sleep). Some patients with sleepwalking also smiled and laughed during N2 sleep and N3 parasomnia. Half of the patients with REM sleep behaviour disorder smiled and one‐third laughed, mostly during REM sleep. The 173 happy faces included mild smiles (24.8%), open‐mouth smiles (29.5%) and laughs (45.7%). More than half of the smiles were the Duchenne (genuine) type, including an active closure of the eyelids. Approximately half of the smiles and laughs were temporally associated with rapid eye movements. There was no increased heart rate variability during smiles and laughs. Two scenic behaviours including smiles and laughs suggested that the happy facial expression was associated with a happy dreaming scenario. Smiling and laughing occasionally persist during adult sleep. There are several lines of evidence suggesting that these happy emotional expressions reflect a true inner mirth. [ABSTRACT FROM AUTHOR]

The reference standard for sleep classification uses manual scoring of polysomnography with fixed 30‐s epochs. This limits the analysis of sleep pattern, structure and, consequently, detailed association with other physiologic processes. We aimed to improve the details of sleep evaluation by developing a data‐driven method that objectively classifies sleep in smaller time intervals. Two adaptive segmentation methods using 3, 10 and 30‐s windows were compared. One electroencephalographic (EEG) channel was used to segment into quasi‐stationary segments and each segment was classified using a multinomial logistic regression model. Classification features described the power in the clinical frequency bands of three EEG channels and an electrooculographic (EOG) anticorrelation measure for each segment. The models were optimised using 19 healthy control subjects and validated on 18 healthy control subjects. The models obtained overall accuracies of 0.71 ± 0.09, 0.74 ± 0.09 and 0.76 ± 0.08 on the validation data. However, the models allowed a more dynamic sleep, which challenged a true validation against manually scored hypnograms with fixed epochs. The automated classifications indicated an increased number of stage transitions and shorter sleep bouts using models with smaller window size compared with the hypnograms. An increased number of transitions from rapid eye movement (REM) sleep was likewise expressed in the model using 30‐s windows, indicating that REM sleep has more fluctuations than captured by today's standard. The models developed are generally applicable and may contribute to concise sleep structure evaluation, research in sleep control and improved understanding of sleep and sleep disorders. The models could also contribute to objective measuring of sleep stability. [ABSTRACT FROM AUTHOR]

Although video polysomnography (vPSG) is not routinely recommended for the evaluation of typical cases of non‐rapid eye movement (NREM) parasomnias, it can aid diagnosis of unusual cases, other sleep disorders and complicated cases with REM behaviour disorder (RBD), and in differentiating parasomnias from epilepsy. In this study, we aimed to assess vPSG findings in consecutive patients with a clinical diagnosis of NREM‐parasomnia covering the whole phenotypic spectrum. Five hundred and twelve patients with a final diagnosis of NREM parasomnia who had undergone vPSG were retrospectively identified. vPSGs were analysed for features of NREM parasomnia and for the presence of other sleep disorders. Two hundred and six (40.0%) patients were clinically diagnosed with sleepwalking, 72 (14.1%) with sleep terrors, 39 (7.6%) with confusional arousals, 15 (2.9%) with sexsomnia, seven (1.4%) with sleep‐related eating disorder, 122 (23.8%) with mixed phenotype, and 51 (10.0%) with parasomnia overlap disorder (POD). The vPSG supported the diagnosis of NREM parasomnia in 64.4% of the patients and of POD in 98%. In 28.9% of the patients, obstructive sleep apnea (OSA) or/and periodic limb movements during sleep (PLMS) were identified, most commonly in older, male, sleepy and obese patients. vPSG has a high diagnostic yield in patients with NREM parasomnia and should be routinely performed when there is diagnostic doubt, or in patients where there is a suspicion of OSA and PLMS. [ABSTRACT FROM AUTHOR]

The article presents an abstract of the study "Polysomnography, power spectra in sleepwalkers - contributions to pathophysiological understanding." The study investigates the segments of polysomnographies of sleepwalkers before and after sleepwalking. The study concludes that the sleepwalking displays some features of rapid eye movement-behavior disorder with an overlap between non-rapid eye movement and rapid eye movement which is potentially dangerous.

The article presents an abstract of the study "Clinical and polysomnographic results in sleepwalkers - implications for pathomechanisms." The study investigates the number of arousal, number of stage shifts, time from rapid eye movement (REM) sleep to sleepwalking and from sleepwalking to next REM in the segments of polysomnographies. The study concludes that sleepwalking is a disorder that occurs near REM and frequently associated with other parasomnias.

The article presents an abstract of the study "Genetic Susceptibility to Sleepwalking: A Candidate Gene Approach," by Michel Lecendreux. It uses a collaborative project on the genetic basis since sleepwalking known as a common parasomnia with high genetic load that may be misdiagnosed as autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE). It suggests that DQB1∗ 05 could be susceptible to sleepwalking especially in familial form, while CHRNA4 does not seem to be associated.

The article presents an abstract of the study "Sleepwalking in a Child With Delayed Sleep Phase Syndrome." In the study, polysomnograph showed severely restricted and deep sleep without any episodes of sleepwalking. Phototherapy successfully advanced the nine-year-old female sleepwalker with delayed sleep phase syndrome. The study reveals that light therapy advance the circadian system of sleep phase syndrome.

The article presents an abstract of the study about sleep architecture differences betweeen the sleepterror and sleepwalker patients and matched controls. The researchers found out that sleep on non-event is abnormal. The results strongly suggest that there is an ongoing arousal process that fragments NREM-SWS whereas rapid-eye-movement sleep in majority of patients is essentially intact.

The article presents the abstract of "Adult Sleepwalking: Clinical, Neurophysiological, and Neuroimaging findings." It focuses on the study which aims to explore the concept of adult sleepwalking (SW). To get some pertinent data, records of adult patients suffering from adult SW were reviewed and reexamined. Other patients were likewise assessed through personal interviews. After data gathering, it was concluded that adult SW is more common than usually thought and may occur in adulthood.

The article presents the abstract of "Study of GABAC Receptor Antagonist on Sleep-Walking Behavior in Rats." It examines the role of gamma-aminobutyric acid type C receptor (GABAC) in the sleep-walking cycle regulation of rats. An overview of the materials, methods and result of the study conducted is discussed.